KOLANTICON GEL

Indications

• Symptomatic relief of gastrointestinal disorders characterized by smooth muscle spasm
• Irritable bowel syndrome
• Acute spasm in diagnostic procedures

Dosage

Children: Child 12–17 years: 10–20 mg three times a day. Child 2–4 years: 5 mg three to four times a day. Child 1 month–1 year: 300–500 micrograms/kg three to four times a day (maximum per dose 5 mg).

Adults: 10–20 mg three times a day, increased if necessary up to 20 mg four times a day; maximum daily dose is 100 mg.

Mechanism of action

Dicycloverine hydrochloride functions as an antimuscarinic by blocking the action of acetylcholine at muscarinic receptors in the smooth muscles of the gastrointestinal tract. This inhibition results in reduced motility and relaxation of the gastrointestinal smooth muscle, alleviating spasms and cramping.

Pharmacodynamics

The primary effect of dicycloverine hydrochloride is the reduction of gut motility due to its antimuscarinic properties. It has a less pronounced antimuscarinic action compared to atropine but may also exhibit some direct relaxant effects on smooth muscle. This dual action helps in relieving abdominal pain associated with smooth muscle spasms.

Pharmacokinetics

Dicycloverine hydrochloride is well absorbed from the gastrointestinal tract. Its onset of action typically occurs within 30 minutes to 1 hour after oral administration, with a duration of effect lasting several hours. The drug undergoes hepatic metabolism and has a variable elimination half-life. Its clearance may be affected by renal function, and caution is advised in patients with renal impairment.

Contra-indications

• Hypersensitivity to dicycloverine or any of its components
• Glaucoma
• Myasthenia gravis
• Severe ulcerative colitis
• Obstructive uropathy
• Severe gastrointestinal obstruction

Adverse effects

• Dry mouth
• Dizziness
• Constipation
• Drowsiness
• Nausea
• Blurred vision
• Urinary retention
• Increased heart rate
• Skin reactions (e.g., flushing, urticaria)

Interactions

• Anticholinergic drugs may enhance effects
• Potentiation of the effects of other CNS depressants such as alcohol
• Antacids containing aluminium may increase risk of toxicity

Precautions

• Use with caution in patients with renal impairment
• May exacerbate conditions like glaucoma and myasthenia gravis
• Monitor for signs of anticholinergic syndrome

Pregnancy

Not known to be harmful; manufacturer advises use only if essential.

Breast-feeding

Avoid; present in milk with potential for causing apnoea in infants.

Storage

Store in a cool, dry place away from direct sunlight. Keep out of reach of children.

Formulations

• Oral solution: Dicycloverine hydrochloride 500 micrograms per 1 ml
• Combination products containing aluminium hydroxide and simeticone

Indications

• Dyspepsia
• Peptic ulcer disease
• Gastroesophageal reflux disease (GERD)
• Heartburn
• Diarrhea
• Mucosal irritations

Dosage

Children: Refer to the BNF for Children for appropriate dosing guidelines.

Adults: Refer to the BNF for specific dosing recommendations based on the condition being treated.

Mechanism of action

Aluminum acts as an astringent, causing local shrinkage or constriction of body tissues through osmotic flow of fluids away from the area of application. This mechanism assists in reducing mucous secretions and managing conditions such as peptic ulcers and diarrhea. Additionally, it can help in drying and hardening of tissues when applied topically.

Pharmacodynamics

Aluminum-based antacids work by neutralizing gastric acid, leading to an increase in gastric pH. This action helps to alleviate symptoms associated with excess gastric acid, such as heartburn and discomfort. The astringent properties of aluminum also contribute to its therapeutic effects in managing mucosal irritations and secretions.

Pharmacokinetics

Aluminum is absorbed minimally when taken orally, with a bioavailability of about 0.1 to 0.5%. The majority of aluminum is excreted renally, and its half-life can be prolonged in individuals with renal impairment. Long-term use may lead to accumulation and potential toxicity, particularly impacting bone and neurological health.

Interactions

• aluminiumhydroxide+deferasirox: Severe (decreases exposure)
• aluminiumhydroxide+enteralfeeds: Unknown (increases risk of blocked enteral or nasogastric tubes)
• aluminiumhydroxide+roxadustat: Unknown (decreases exposure)

Pregnancy

Aluminum compounds are generally considered safe in pregnancy when used as directed. However, excessive exposure should be avoided.

Breast-feeding

Aluminum is excreted in breast milk; caution is advised when administered to nursing mothers.

Storage

Store in a cool, dry place, away from direct sunlight.

Formulations

• aluminium hydroxide suspension
• aluminium hydroxide tablets

Indications

• Irritable bowel syndrome (IBS)
• Gastrointestinal spasm
• Abdominal cramping

Dosage

Children: Refer to the BNF for Children for specific dosing information.

Adults: 20 mg to 40 mg orally, 4 times daily or 10 mg to 20 mg by intramuscular injection, as needed. Do not administer intravenously.

Mechanism of action

Dicyclomine achieves its action partially through direct antimuscarinic activity at the M1, M3, and M2 receptors, and partially through antagonism of bradykinin and histamine. It non-competitively inhibits the action of bradykinin and histamine, leading to a direct relaxant effect on smooth muscle, specifically reducing the strength of contractions observed in ileal spasms. Its major action appears to be a nonspecific direct relaxant effect on smooth muscle rather than competitive antagonism of acetylcholine.

Pharmacodynamics

Dicyclomine is classified as an anticholinergic agent that relaxes the smooth muscles of the intestines. Its duration of action is relatively short, leading to a typical administration schedule of four times daily, with doses ranging from 20-40 mg orally or 10-20 mg via intramuscular injection. It is important to note that dicyclomine should not be administered intravenously.

Pharmacokinetics

Dicyclomine is absorbed through the gastrointestinal tract and metabolized in the liver. The onset of action occurs within 1 hour of administration, with peak effects seen at approximately 1-2 hours. The elimination half-life varies, but it is generally in the range of 1-2 hours, necessitating multiple daily doses to maintain therapeutic levels. The drug is primarily excreted in urine as metabolites.

Contra-indications

• Glaucoma
• Myasthenia gravis
• Severe ulcerative colitis
• Obstructive uropathy
• Obstructive gastrointestinal disease
• Tachyarrhythmias

Adverse effects

• Dizziness
• Dry mouth
• Nausea
• Vomiting
• Constipation
• Blurred vision
• Tachycardia
• Urinary retention

Interactions

• Clozapine (unknown additive effect)
• Second-generation antipsychotics (unknown additive effect)

Precautions

• Use with caution in patients with renal impairment
• Use with caution in patients with hepatic impairment
• Caution in elderly patients due to increased risk of sensitivity to anticholinergic effects

Pregnancy

Dicyclomine is not recommended during pregnancy due to potential risk to the fetus.

Breast-feeding

Dicyclomine is excreted in breast milk and may cause adverse effects in nursing infants; use with caution.

Storage

Store at room temperature, away from light and moisture. Keep out of reach of children.

Formulations

• Oral tablet (20 mg, 40 mg)
• Injection (10 mg, 20 mg)

Dosage

Children: Refer to specific guidelines for pediatric dosing; consult the BNF for Children for accurate dosage information.

Adults: Refer to specific guidelines for use; dosage may vary based on the context of use.

Mechanism of action

Hydroxide ions act primarily as bases, neutralizing acids to form water and salts. They participate in various biochemical pathways, including selenium metabolism and the degradation of reactive oxygen species. Hydroxide can influence enzyme activity and stability by altering the pH of the environment, thereby affecting metabolic reactions.

Pharmacodynamics

Hydroxide ions can impact biological processes by changing the local pH, which influences enzyme activity, ion transport, and the solubility of other compounds. Their ability to neutralize acids can help regulate physiological pH, contributing to homeostasis in living organisms.

Pharmacokinetics

As an inorganic ion, hydroxide does not undergo traditional pharmacokinetic processes like absorption, distribution, metabolism, or excretion. Instead, it is rapidly equilibrated in biological fluids and participates in acid-base reactions, having immediate effects on the local environment.

Pregnancy

There is limited information regarding the use of hydroxide during pregnancy. Consult a healthcare professional for advice.

Breast-feeding

Limited data is available on the excretion of hydroxide in breast milk. Consult a healthcare professional before use.

Storage

Store in a cool, dry place away from direct sunlight. Keep out of reach of children.

Indications

• Vision correction
• Phototherapy for skin conditions (e.g., psoriasis, eczema)
• Treatment of seasonal affective disorder (SAD)
• Circadian rhythm disorders
• Wound healing

Dosage

Children: Light therapy for paediatric patients should be approached with caution and always under professional guidance. Specific dosages will depend on the individual treatment protocol and condition being addressed.

Adults: Dosage of light therapy varies based on the condition being treated and should be tailored to individual needs, typically ranging from 15 minutes to 2 hours of exposure per day depending on the specific treatment protocol.

Mechanism of action

Light affects biological systems primarily through phototransduction, which involves the conversion of light into electrical signals within photoreceptor cells in the retina. This process initiates a cascade of biochemical reactions that ultimately lead to visual perception. In addition, specific wavelengths of light can interact with various biological molecules, triggering cellular responses such as the production of vitamin D through skin exposure to UVB radiation.

Pharmacodynamics

The pharmacodynamic effects of light are highly dependent on its wavelength and intensity. Short-wavelength blue light (around 480 nm) is known to influence circadian rhythms by affecting melatonin secretion. In therapeutic settings, light can modulate biological responses, such as promoting wound healing, reducing inflammation, and alleviating symptoms of seasonal affective disorder (SAD) through bright light therapy.

Pharmacokinetics

Light does not undergo traditional pharmacokinetic processes such as absorption, distribution, metabolism, or excretion. Instead, its effects are immediate and localized, depending on the intensity and duration of exposure. The penetration depth of light varies with wavelength; for example, UV light can penetrate the skin and affect deeper tissues, while visible light primarily affects the surface layers.

Pregnancy

There is limited data on the effects of light exposure during pregnancy. However, excessive exposure to bright light can be harmful to both the mother and the developing fetus.

Breast-feeding

Light exposure is generally considered safe while breastfeeding, but excessive exposure should be avoided to prevent potential harm to the infant.

Storage

Light should be properly controlled and managed in environments where it is used, ensuring that exposure levels are safe and effective.

Mechanism of action

Oxides do not have a single mechanism of action as they are a broad category of compounds. However, in general, metal oxides can exhibit catalytic properties, while non-metal oxides may participate in biochemical reactions by forming acids or bases upon dissolution in water.

Pharmacodynamics

The pharmacodynamics of oxides depend on the specific type of oxide and its interaction with biological systems. For instance, metal oxides may have antimicrobial properties, while certain non-metal oxides can influence metabolic pathways through their acid-base chemistry. The effects vary widely, necessitating specific studies for each oxide's role in therapeutic contexts.

Pharmacokinetics

The pharmacokinetics of oxides are also variable. Many metal oxides are poorly soluble and thus have limited absorption when ingested. Non-metal oxides, such as carbon dioxide, can be readily absorbed and utilized in metabolic processes. The distribution, metabolism, and excretion of oxides depend on their chemical form and the biological system in which they are involved.

Pregnancy

Not applicable as oxide is not a drug but a class of chemical compounds.

Breast-feeding

Not applicable as oxide is not a drug but a class of chemical compounds.

Storage

Store in a cool, dry place away from direct sunlight.

Indications

• Flatulence
• Bloating
• Gastroesophageal reflux disease
• Functional dyspepsia

Dosage

Children: For children, refer to the BNF for Children for specific dosing recommendations.

Adults: The usual adult dose is 40 to 125 mg taken after meals and at bedtime, as needed.

Mechanism of action

Simethicone is a surfactant that decreases the surface tension of gas bubbles in the gastrointestinal tract, facilitating their expulsion. It acts by forming a film of low surface tension that promotes the coalescence of mucus-surrounded gas bubbles, allowing for easier passage of gas.

Pharmacodynamics

Simethicone decreases the surface tension of gas bubbles in the gastrointestinal tract, facilitating their expulsion. Its effects are generally short-lived, as it is typically administered as needed. The therapeutic index is wide since it is not absorbed systemically, making it safe for use in various patient populations.

Pharmacokinetics

Simethicone is not systemically absorbed following oral administration, which contributes to its safety profile. Due to its lack of systemic absorption, specific pharmacokinetic parameters such as half-life, clearance, and volume of distribution are not applicable.

Pregnancy

Simethicone can be used during pregnancy as there are no known risks associated with its use.

Breast-feeding

Simethicone is considered safe to use during breastfeeding, as it is not absorbed systemically.

Storage

Store in a cool, dry place, away from direct sunlight. Keep out of reach of children.

Formulations

• Oral suspension
• Chewable tablets
• Soft gels

Mechanism of action

Aluminum Acetate is an astringent. An astrignent is a chemical that tends to shrink or constrict body tissues, usually locally after topical medicinal application. The shrinkage or constriction is through osmotic flow of water (or other fluids) away from the area where the astringent was applied. Astringent medicines cause shrinkage of mucous membranes or exposed tissues and are often used internally to check discharge of blood serum or mucous secretions. This can happen with a sore throat, hemorrhages, diarrhea, or with peptic ulcers. Externally applied astringents, which cause mild coagulation of skin proteins, dry, harden, and protect the skin. Acne sufferers are often advised to use astringents if they have oily skin. Astringents also help heal stretch marks and other scars. Mild astringent solutions are used in the relief of such minor skin irritations as those resulting from superficial cuts, allergies, insect bites, or fungal infections such as athlete's foot. Excessive dietary aluminum has been proposed to be a factor contributing to several neurological disorders in humans. Six 8-week-old female Swiss Webster mice were fed for 10 wk purified diets containing 100 (control), 500 or 1000 ug aluminum/g diet. Brain and liver lipid peroxidation was determined by evaluating the production of 2-thiobarbituric acid reactive substances in brain and liver homogenates in the presence or absence of 50 uM ferrous iron. 2-Thiobarbituric acid reactive substances production in the absence of iron in brain homogenates from mice fed the 1000 ug/g diet was higher (30%) than that in the 100 ug/g control group (3.1 vs 2.4 nmol 2-thiobarbituric acid reactive substances/mg protein). The addition of ferrous iron increased 2-thiobarbituric acid reactive substances production in brain homogenates from all 3 dietary groups. The iron induced 2-thiobarbituric acid reactive substances production was 26% higher in the 1000 ug/g brain homogenates than in the 100 ug/g group (4.9 vs 3.9 nmol 2-thiobarbituric acid reactive substances/mg protein). Brain 2-thiobarbituric acid reactive substances production in the presence and absence of iron was similar between the 100 and 500 ug/g aluminum groups. 2-Thiobarbituric acid reactive substances production in liver homogenates measured either with or without iron was similar for the 3 groups. These results show that, in mice, dietary aluminum intoxication leads to increased brain 2-thiobarbituric acid reactive substance production, suggesting that enhanced lipid peroxidation may be one possible mechanism underlying the neurological damage associated with increased tissue aluminum. Evidence is presented indicating that dementias are associated with a relative insufficiency of magnesium in the brain. Such insufficiency may be attributable to low intake or retention of magnesium; high intake of a neurotoxic metal, such as aluminum, which inhibits activity of magnesium requiring enzymes; or impaired transport of magnesium and/or enhanced transport of the neurotoxic metal into brain tissue. It is proposed that Alzheimer's disease involves a defective transport process, characterized by both an abnormally high incorporation of aluminum and an abnormally low incorporation that an altered serum protein contributes to the progression of Alzheimer's disease by having a greater affinity for aluminum than for magnesium, in contrast to the normal protein, which binds magnesium better than aluminum. The altered protein crosses the blood-brain barrier more efficiently than the normal protein and competes with the normal protein in binding to brain neurons. Binding of the altered protein to the target neurons would both facilitate aluminum uptake and impede magnesium uptake. Evidence suggests that albumin is the serum protein that is altered. Aluminum is established as a neurotoxin, although the basis for its toxicity is unknown. It recently has been shown to alter the function of the blood-brain barrier, which regulates ex

Mechanism of action

Dicyclomine achieves its action partially through direct antimuscarinic activity of the M1, M3, and M2 receptors; and partially through antagonism of bradykinin and histamine. Dicyclomine non-competitively inhibits the action of bradykinin and histamine, resulting in direct action on the smooth muscle, and decreased strength of contractions seen in spasms of the ileum. ...MAJOR ACTION APPEARS TO BE NONSPECIFIC DIRECT RELAXANT ACTION ON SMOOTH MUSLCE RATHER THAN COMPETITIVE ANTAGONISM OF ACH.

Pharmacodynamics

Dicyclomine is an anticholinergic drug used to relax the smooth muscles of the intestines. It's duration of action is not especially long as it is usually taken 4 times daily with individual doses of 20-40mg orally or 10-20mg by intramuscular injection. Dicyclomine should not be administered intravenously.

Mechanism of action

Simethicone is a surfactant that decreases the surface tension of gas bubbles in the gastrointestinal tract, more easily allowing gas to exit the body. The clinical use of simethicone is based on its antifoam properties. Silicone antifoams spread on the surface of aqueous liquids, forming a film of low surface tension and thus causing collapse of foam bubbles. Simethicone reportedly allows mucus-surrounded gas bubbles in the GI tract to coalesce and be expelled.

Pharmacodynamics

Simethicone decreases the surface tension of gas bubbles in the gastrointestinal tract, facilitating their expulsion. It has a short duration of action as it is generally given as needed, and a wide therapeutic index as it is not systemically absorbed.